2005 Fiscal Year Final Research Report Summary
Analysis of molecular and genetic mechanism in the pathogenesis of COPD and bronchial asthma
| Project/Area Number |
15390260
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Nihon University |
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Principal Investigator |
HASHIMOTO Shu Nihon University, School of Medicine, Lecture, 医学部, 講師 (30159090)
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| Co-Investigator(Kenkyū-buntansha) |
SHIMIZU Kazufumi Nihon University, School of Medicine, Professor, 教授 (50004677)
KABAYASHI Tomoko Nihon University, School of Medicine, Lecture, 助手 (10343576)
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| Project Period (FY) |
2003 – 2005
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| Keywords | COPD / bronchial asthma / MAP kinase / ASK1 / A20 / toll-like receptor |
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| Research Abstract |
This project has attempted to clarify the molecular mechanism and genetic background in the pathogenesis of chronic obstructive pulmonary disease (COPD) and bronchial asthma. It has been demonstrated that various inflammatory cells and mediators, and oxidative stresses are involved in the pathogenesis of these diseases. In addition, airway infection such as bacterial and viral infection play a role in the pathogenesis, progression and modification of these diseases. This project have shown that 1)a role of mitogen-activated protein kinase (MAPK) in airway inflammation via toll-like receptor(TLR)-2 and -4-dependent activation, 2)a role of oxidative stress-sensitive signaling molecule, ASK-1 in airway inflammation using ASK-1 knockout mice, 3)a role of endogenous anti-inflammatory molecules, A20, in airway inflammation in vitro and in vivo. In conclusion, for attenuating the airway inflammation seen in COPD and bronchial asthma, ASK-1 could be a molecular target for the therapy. Furtherm
… More
ore, A20 could be useful molecule to control the excessive inflammation. This project has attempted to clarify the molecular mechanism and genetic background in the pathogenesis of chronic obstructive pulmonary disease (COPD) and bronchial asthma. It has been demonstrated that various inflammatory cells and mediators, and oxidative stresses are involved in the pathogenesis of these diseases. In addition, airway infection such as bacterial and viral infection play a role in the pathogenesis, progression and modification of these diseases. This project have shown that 1)a role of mitogen-activated protein kinase (MAPK) in airway inflammation via toll-like receptor (TLR)-2 and -4-dependent activation, 2)a role of oxidative stress-sensitive signaling molecule, ASK-1 in airway inflammation using ASK-1 knockout mice, 3)a role of endogenous anti-inflammatory molecules, A20, in airway inflammation in vitro and in vivo. In conclusion, for attenuating the airway inflammation seen in COPD and bronchial asthma, ASK-1 could be a molecular target for the therapy. Furthermore, A20 could be useful molecule to control the excessive inflammation. Less
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[Journal Article] An inhibitory effect of A20 on NE-kB activation in airway epithelium upon influenza virus infection.2006
Author(s)
Onose A, Hashimoto_S, Hayashi S, Maruoka S, Kumasawa F, Mizumura K, Jibiki I, Matsumoto K, Gon Y, Kobayashi T, Takahashi N, Shibata Y, Abiko Y, Shibata T, Shimizu K, Horie T.
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Journal Title
Eur J Pharmacol. (Accepted for the publication)
Description
「研究成果報告書概要(欧文)」より
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[Journal Article] Apoptosis signal-regulating kinase 1 in leukotriene D(4)-induced activator protein-1 activation in airway smooth muscle cells.2005
Author(s)
Kumasawa F, Hashimoto S, Onose A, Jibiki I, Mizumura K, Matsumoto K, Maruoka S, Gon Y, Kobayashi T, Takahashi N, Ichijo H, Horie T.
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Journal Title
Eur J Pharmacol. 517(1-2)
Pages: 11-16
Description
「研究成果報告書概要(欧文)」より
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